Month: September 2017

The safety of electronic cigarettes is a widely debated issue. The latest research demonstrates that in people who do not smoke, they can alter heart rate variability, which is an indicator of increased adrenaline levels.

Introduced in 2007, electronic cigarettes (e-cigarettes) are now “the fastest-rising tobacco product in the United States.”

There is little doubt that these devices deliver fewer carcinogens to the user, but, because they often contain nicotine, conversations regarding their safety are ongoing.

On the one hand, e-cigarettes offer a relatively safe option for nicotine-addicted individuals. On the other hand, they are seen by some as a new route to addiction with health concerns of their own.

Research published this week in the Journal of the American Heart Association investigates the potential heart health implications of non-smokers using nicotine-based e-cigarettes.

Lead study author Dr. Holly Middlekauff, of the University of California, Los Angeles, says, “While e-cigarettes typically deliver fewer carcinogens than are found in the tar of tobacco cigarette smoke, they also usually deliver nicotine.”

“Many believe that the tar – not the nicotine – is what leads to increased cancer and heart attackrisks. So, we asked the question, are e-cigarettes safe?”

E-cigarettes and the sympathetic response

Nicotine is not a carcinogen, but it is still a drug. It is a sympathomimetic, which is a compound that mimics the sympathetic nervous system, increasing adreline levels in circulation and raising heart rate and blood pressure. These are physiological changes associated with the “fight or flight” response.

It is this activation of the sympathetic nervous system and the influx of adrenaline that worries some medical researchers. These types of actions are, over the long-term, linked with increased cardiovascular risk.

Cardiac sympathetic nerve activity can be measured noninvasively using a heart monitor to detect heart rate variability (HRV), which is the variability in the duration between heartbeats. This measure can be used as a predictor of cardiovascular disease; lower HRV increases risk.

This rise in cardiac sympathetic nerve activity and its associated rise in circulating adrenaline, combined with a lack of long-term data on e-cigarettes, creates concern as to their overall safety.

In other research, Dr. Middlekauff’s team showed that chronic e-cigarette use contributed to increased resting cardiac sympathetic nerve activity.

The current study was designed to find out whether this effect could be seen in acute, or short-term, use of e-cigarettes, and whether it is due to nicotine or other ingredients present in the devices – such as propylene glycol and vegetable glycerin.

E-cigarettes, nicotine, and cardiac risk

In total, 33 healthy volunteers – none of whom smoke cigarettes or e-cigarettes – were involved in the study. Each participant, on separate days, smoked an e-cigarette with nicotine, one without nicotine, and a sham (empty) e-cigarette.

According to the study authors, this is the first study of its kind to separate the nicotine from the non-nicotine components of e-cigarettes in this way.

For each individual, HRV was measured. A blood sample was also taken to assess oxidative stressby measuring levels of an enzyme called plasma paraoxonase.

After analysis, the team found that HRV was significantly altered when individuals used the nicotine e-cigarette but not in the non-nicotine and sham conditions. However, they saw no significant differences in markers of oxidative stress.

Dr. Middlekauff explains how the findings add to the body of evidence against nicotine as a safe drug. “While it’s reassuring that the non-nicotine components do not have an obvious effect on adrenaline levels to the heart,” she says, “these findings challenge the concept that inhaled nicotine is benign or safe.”

She says, “Our study showed that acute electronic cigarette use with nicotine increases cardiac adrenaline levels. And, it’s in the same pattern that is associated with increased cardiac risk in patients who have known cardiac disease, and even in patients without known cardiac disease.”

Limitations and future research

The study has limitations; it included only a small number of participants and studied just one of the thousands of e-cigarette fluids. For this reason, the authors are keen to extend their findings.

“I think that just seeing this pattern at all is very concerning and it would hopefully discourage non-smokers from taking up electronic cigarettes.”

Dr. Holly Middlekauff

In the future, the researchers plan to continue their studies – the team would like to investigate this effect in habitual e-cigarette smokers and take a more in-depth look at the potential role of oxidative stress.

The current findings are likely to intensify an already intense debate. The take-home message is that e-cigarettes are less likely to cause cancer, but they are not without their own dangers.

A new study of people living in Sweden has found that children with inflammatory bowel disease have a higher risk of cancer – especially gastrointestinal cancers – both in childhood and in later life, compared with individuals without the disease.

The international team of researchers, including members of the Karolinska Institutet in Sweden, report the findings in the BMJ.

They note that the raised risk of cancer for children with inflammatory bowel disease (IBD) carries on into adulthood and has not reduced following the introduction of new ways to manage the disease, such as with biological agents.

They also point out that, while they found a higher relative risk of cancer, the absolute risks are low. Compared with healthy individuals, there was one extra case of cancer for every 556 people with IBD followed for 1 year.

IBD results from chronic inflammation of the gut, or gastrointestinal (GI) tract. It can strike at any age, but most people who are diagnosed are between 15 and 40 years old.

There are two types of IBD: Crohn’s disease and ulcerative colitis. While they share some features, there are also some key differences.

For example, in Crohn’s disease, the inflammation affects any region of the GI tract between the mouth and the anus and can occur in all layers of the tissue. In ulcerative colitis, however, the disease affects the colon and the rectum and tends only to occur in the innermost layer of tissue.

IBD is classed as an autoimmune disorder – that is, a disease that arises when the immune system mistakenly attacks the body’s own tissue: in this case, the gut.

The exact causes of IBD are still unknown, but scientists suggest that environmental factors might trigger the disease in people whose genetic makeup makes them more susceptible to it.

In the United States, around 3 million people (or 1.3 percent of adults) reported having received a diagnosis of Crohn’s disease or ulcerative colitis in 2015.

A new study of people living in Sweden has found that children with inflammatory bowel disease have a higher risk of cancer – especially gastrointestinal cancers – both in childhood and in later life, compared with individuals without the disease.

The international team of researchers, including members of the Karolinska Institutet in Sweden, report the findings in the BMJ.

They note that the raised risk of cancer for children with inflammatory bowel disease (IBD) carries on into adulthood and has not reduced following the introduction of new ways to manage the disease, such as with biological agents.

They also point out that, while they found a higher relative risk of cancer, the absolute risks are low. Compared with healthy individuals, there was one extra case of cancer for every 556 people with IBD followed for 1 year.

IBD results from chronic inflammation of the gut, or gastrointestinal (GI) tract. It can strike at any age, but most people who are diagnosed are between 15 and 40 years old.

There are two types of IBD: Crohn’s disease and ulcerative colitis. While they share some features, there are also some key differences.

For example, in Crohn’s disease, the inflammation affects any region of the GI tract between the mouth and the anus and can occur in all layers of the tissue. In ulcerative colitis, however, the disease affects the colon and the rectum and tends only to occur in the innermost layer of tissue.

IBD is classed as an autoimmune disorder – that is, a disease that arises when the immune system mistakenly attacks the body’s own tissue: in this case, the gut.

The exact causes of IBD are still unknown, but scientists suggest that environmental factors might trigger the disease in people whose genetic makeup makes them more susceptible to it.

In the United States, around 3 million people (or 1.3 percent of adults) reported having received a diagnosis of Crohn’s disease or ulcerative colitis in 2015.

Their analysis included 9,405 people with childhood-onset IBD and 92,870 individuals from the general population matched for birth year, age, sex, and place of residence.

The researchers calculated the risk of cancer in the two groups before the age of 18, before age 25, and over the whole study period – from 1964 to 2014 – up to an average age of 30 years.

After excluding the effect of other factors that might influence the result, the team found 497 first cancers in people with childhood-onset IBD, which is equivalent to a rate of 3.3 per 1,000 person-years. This compared with 2,256 cancers in the matched individuals, which is equivalent to 1.5 per 1,000 person-years.

“This corresponds to one extra case of cancer for every 556 patients with inflammatory bowel disease followed for a year, compared with reference individuals,” they note.

Higher cancer risk persists over time

The team also found that the cancer risk increased in the first year following IBD diagnosis and stayed high over 5 years of follow-up and beyond. This was especially the case for cancers of the colon, rectum, small intestine, and liver.

Risk factors for any cancer linked to childhood-onset IBD included long-standing colitis, chronic liver disease, and a family history of early-onset cancer.

The authors note that they do not rule out that drugs may be a factor in the higher risk of cancer in childhood-onset IBD, but they explain that their study was “not big enough” to assess this.

However, they do suggest that the main driver underlying the higher risk of cancer could be the “extent and duration of chronic inflammation” of the IBD.

They also emphasize that because this was an observational study, it could not determine whether IBD causes cancer.

Nevertheless, the researchers suggest that the study’s biggest strength is the large number of participants. They also outline some weaknesses, such as the fact that they had no information about smoking or about “disease severity, disease extent, or disease behavior.”

They conclude, “Childhood-onset inflammatory bowel disease is associated with an increased risk of any cancer, especially gastrointestinal cancers, both during childhood and later in life. The higher risk of cancer has not fallen over time.”

Much larger studies now needed

In a linked editorial, Susan Hutfless – who is an associate professor of medicine at Johns Hopkins University in Baltimore, MD – acknowledges that people with IBD “worry about developing cancer,” but she urges them and their families “to focus on the very low incidence of cancer in childhood.”

The study “sets an excellent example” of how to investigate the link between IBD and cancer, Prof. Hutfless notes. However, she points out that only very much larger studies can address questions such as whether IBD drugs raise cancer risk, and the best way to go about cancer surveillance in patients with IBD.

She describes the study as a “thoughtful and thorough investigation” and says that it “confirms the need for international collaboration in the study of cancer surveillance” for children diagnosed with IBD.

As the investigators themselves point out, Prof. Hutfless notes that better surveillance of IBD could lead to better detection, earlier diagnosis, and higher reported rates of cancer. “The ultimate goal of surveillance,” she adds, “is of course reduced cancer mortality, an outcome that requires very long follow-up.

Essential oils are used as home remedies for a variety of ailments. But is using essential oils an effective way to relieve headaches, and, if so, which essential oils are best?

An essential oil is a concentrated liquid extracted from a plant. Aromatherapy is an alternative therapy based on the use of these oils. Aromatherapists believe that each essential oil offers a different set of health benefits.

Research supports the health benefits of certain essential oils, while other claims are based on tradition. This article explores five of the best essential oils for treating headaches, as supported by scientific evidence.

Overview

It is estimated that more than half of the adult population worldwide experiences occasional headaches, with the most common type being a tension headache.

While there are a number of over-the-counter and prescription medications available for headaches, these treatments can cause side effects.

When someone experiences headaches regularly, they may look for natural treatments, including essential oils.

Which essential oils help headaches?

There are a number of studies that show specific essential oils may be beneficial for headaches. These include:

1. Lavender oil

Lavender is often used to help people get to sleep and to reduce stress, anxiety, or depression.

Many believe that it can help relieve headaches and migraines that are triggered by stress.

A 2012 study suggests that the inhalation of lavender essential oil can be a safe and effective treatment to manage migraine headaches.

2. Rosemary oil

Rosemary oil is traditionally used to treat headaches and improve circulation.

There are few studies that specifically support rosemary oil as an effective headache treatment. However, a 2008 study suggests that rosemary oil has anti-inflammatory and pain-killing properties.

Another study from 2013 found that rosemary oil helped to reduce pain and insomnia in people going through opium withdrawal treatment.

These research examples suggest that rosemary oil may reduce the pain associated with a headache. However, more studies on humans are required before this can be confirmed.

3. Peppermint oil

Peppermint has been used in alternative medicines for thousands of years. It is one of the most popular essential oils for treating headaches.

A recent 2015 review of published studies on essential oils states that applying peppermint oil to the temples and forehead provides relief from tension headaches.

The active ingredient in peppermint oil is menthol. Research published in 2015 shows menthol may be effective in treating migraines when applied to the head as a gel.

4. Chamomile oil

People traditionally drink chamomile tea to relax and unwind. Chamomile oil is commonly believed to have a similar effect.

Research from 2012 showed that chamomile oil might improve some of the symptoms of anxiety and depression.

As headaches are often caused by stress and anxiety, it follows that chamomile oil may help treat headaches.

There are anti-inflammatory properties in chamomile that may also reduce a headache, but more research is needed into its health benefits.

5. Eucalyptus oil

Eucalyptus is traditionally used to clear sinuses and reduce inflammation. People experiencing headaches due to blocked sinuses may find that inhaling eucalyptus reduces their symptoms.

One study found that eucalyptus oil was effective for relieving pain and lowering blood pressurewhen it was inhaled.

How to use essential oils for headaches

There are a number of different ways that you can use essential oils to treat a headache. These include:

Applying oil to the temples or forehead: Essential oils need to be diluted with a carrier oil, such as coconut oil, before they can be applied to the skin. Once diluted, the oil can be massaged into the temples and across the forehead.

Inhaling oil: Essential oils can be inhaled by adding a few drops to a tissue, holding the tissue under the nose and breathing deeply.

Using a compress: Create a compress by soaking a towel in cold water with a few drops of essential oil. The compress can be applied to the forehead or neck.

Adding oil to the bath: Adding a few drops of essential oil to a hot bath can be a relaxing way to treat a headache.

Researchers from Duke University in Durham, NC, may have discovered a new way of killing off cancer cells.

The team was jointly led by Dr. Matthias Gromeier, a professor in the Department of Neurosurgery, and Prof. Smita Nair, who is an immunologist in the Department of Surgery.

The new research – which is published in the journal Science Translational Medicine – shows how a modified poliovirus enables the body to use its own resources to fight off cancer. The modified virus bears the name of recombinant oncolytic poliovirus (PVS-RIPO).

PVS-RIPO has been in clinical trials since 2011 and preliminary results have offered hope to patients with one of the most aggressive forms of brain tumor: recurrent glioblastoma. So, the researchers set out to investigate more deeply how exactly PVS-RIPO works.

Explaining the rationale behind their research endeavor, Dr. Gromeier says, “Knowing the steps that occur to generate an immune response will enable us to rationally decide whether and what other therapies make sense in combination with poliovirus to improve patient survival.”

Poliovirus attacks tumors, inhibits regrowth

The researchers examined the behavior of the poliovirus in two human cell lines: melanoma and triple-negative breast cancer. They observed that the poliovirus attaches itself to cancerous cells. These cells have an excess of the CD155 protein, which acts as a receptor for the poliovirus.

Then, the poliovirus starts to attack the malignant cells, triggering the release of antigens from the tumor. Antigens are toxic substances that the body does not recognize, therefore setting off an immune attack against them.

So, when the tumor cells release antigens, this alerts the body’s immune system to start attacking. At the same time, the poliovirus infects the dendritic cells and macrophages.

Dendritic cells are cells whose role it is to process antigens and “present” them to T cells, which are a type of immune cell. Macrophages are another type of immune cell – namely, large white blood cells whose main role is to rid our bodies of debris and toxic substances.

The cell culture results – which the researchers then verified in mouse models – showed that once PVS-RIPO infects the dendritic cells, these cells “tell” T cells to start the immune attack.

Once started, this process seems to be continuously successful. The cancer cells continue to be vulnerable to the immune system’s attack over a longer period of time, which appears to stop the tumor from regrowing.

As Prof. Nair explains, “Not only is poliovirus killing tumor cells, it is also infecting the antigen-presenting cells, which allows them to function in such a way that they can now raise a T cell response that can recognize and infiltrate a tumor.”

“This is an encouraging finding, because it means the poliovirus stimulates an innate inflammatory response.”

“This includes novel combination treatments that we will pursue,” he added.

More specifically, he explains, because the study revealed that after treatment with the poliovirus “immune checkpoints are increased on immune cells,” a future strategy the researchers plan to explore is “[oncolytic] poliovirus combined with immune checkpoint blockade.”

The benefits of restricting calories on health and extending life span are well established.

Fasting has been used for thousands of years for spiritual and health benefits and has become popular in recent times due to the celebrity endorsement of intermittent fasting, aka the ‘5:2 diet’!

Although dietary advice has long focused on eating regular low-fat meals, intermittent fasting and the 5:2’s counterintuitive approach to weight loss has attracted thousands of women and men.

WHAT ARE THE BENEFITS?

It can improve glucose tolerance

Insulin resistance is generally caused as a result of the body’s reduced ability to remove excess glucose from the blood either because insufficient insulin is released or the glucose receptors have become less sensitive.

Excess glucose will be converted to fat and stored in tissues not suitable for fat storage.

As the body uses fat as a fuel during intermittent fasting, fat stores will reduce allowing the cells to regain insulin function and glucose sensitivity.

Studies show that intermittent fasting can improve many health parameters especially in pre-diabetic and insulin resistant people, where a caloric restriction can avoid the need to use medication.

Further findings also suggest that short term intermittent fasting may be a safe and tolerable dietary intervention for those already diagnosed with Type 2 Diabetes and may improve body weight and fasting glucose levels.

It helps to establish a routine

Although it can be difficult to establish a new way of eating in conjunction with family or work commitments at the outset, once you’ve developed a plan that works, tweaking and adjusting to suit your lifestyle, it’ll soon simply become the way you eat, in terms of timings and good quality meal choices.

Understanding your body’s genuine hunger signals and not confusing them with cravings often associated with the consumption of too many processed foods will give you greater understanding of your body and improve your confidence to maintain healthy habits.

Having a regular routine, with strict eating times, can simplify your day to day life especially if you’re feeling good for it.

It improves your skin health

Many skin conditions can be alleviated by eating a good quality diet, high in vegetables and fiber and avoiding processed foods.

To ensure adequate nutrients with intermittent fasting, you will need to avoid these pro-inflammatory foods that offer little nutritive value and in doing so, you will reduce inflammation, often associated with skin conditions such as acne and eczema.

Furthermore, if you suspect your skin condition is exacerbated by a specific food sensitivity or intolerance, eliminating this food during a fast will offer you the opportunity to re-introduce a food one at a time afterwards, to establish if it is the culprit.

It makes you more resistance to health conditions

Intermittent fasting’s ability to reduce weight will result in lower body fat.

This has further benefits to many health outcomes including improving heart function, helping to prevent cancer and generally improved immune health.

It will help you focus

Being in control of regulating your food intake also makes you more aware of your body.

This deepened sense of understanding and connection can help reduce stress and anxiety and allow you to have a clear mind to focus.

HOW YOU CAN MAKE FASTING WORK FOR YOU

Intermittent fasting should be viewed as a long term lifestyle choice rather than a crash diet.

Otherwise, it is likely that you will regain any weight lost if you resume your original eating habits.

It is also essential that you make healthy food choices; ensuring good nutrition is vital when fasting to ensure the body’s processes are taking place efficiently and effectively.

Thus, planning your meals to make sure you are getting adequate nutrients is very important.

There are two ways to successfully achieve this pattern of eating:

The daily approach

The simple concept is to aim to fast every day for 16-18 hours a day and only consume your food in the remaining six to eight hours.

For example, if you eat your evening meal at 6pm, then you would not eat your next meal until at least 12pm the following day, allowing an 18-hour fast in between.

The weekly approach

This suggests that you eat normally five days a week and diet two, preferably consecutive, days a week, reducing your calorie intake for those two days to a quarter of their normal level (500 calories for women, 600 for men).

As long as you avoid bingeing for five days and starving for the other two, evidence suggests this can be effective as part of a longer-term weight management strategy.

Start gradually

To start with, increase the gap between dinner and breakfast.

If you’re not hungry you could skip breakfast altogether; going from dinner to lunch works best.

Consider the ideal ratio of 16:8 hours, this means you’d be eating a lower-calorie but nutrient dense diet within the eight-hour window.

Typically, this would be from midday until 8pm.

Spread this over two meals and then fast until lunch the following day.

Repeat this routine at least two to three times per week.

If you feel hungry any time outside of the eight-hour window, distract yourself with an activity or task so that you’re not so aware of the hunger pangs.

Factoring in a daily brisk walk will help to speed up your metabolism and maintain muscle mass.

If you’re opting for the weekly approach, do not fast for longer than three days in a row to avoid a significant reduction in your metabolism and to protect against muscle loss.

If you’ve embarked on this approach on a long-term basis, including a cheat day every now and again is not a problem.

WHO SHOULD NOT FAST

1. People who are underweight

Restricting calories may result in further weight loss.

2. Children

Their nutrient and energy requirements are different to adults and fasting may not allow a child to thrive.

3. Pregnant or breast feeding mothers

Pregnancy is a time to ensure good nutrients and adequate calories for a growing baby.

4. If you have an eating disorder

Even if you have struggled with an eating disorder in the past, you may find adopting an eating pattern that restricts food may trigger a relapse.

5. If you’re recovering from surgery

Restricting nutrient intake and energy production may impair repair after surgery.

6. If you are feeling unwell or have a fever

It is important to listen to your body and avoid fasting if your body is not in optimal health.

7. If you are taking any prescribed medications, Type 1 diabetics and diabetics on insulin

It is essential to consult with your GP before embarking on any weight loss program.

The mere act of putting one foot in front of the other for a few minutes can significantly boost our mood, a study has discovered.

And it doesn’t matter where we do it, why we do it, who we do it with, or what effect we expect the walk to have.

Psychologists say the happiness-causing effects arise from the actual physical movement which is connected to how we evolved to move to find food and other rewards.

The researchers say their study is the first to show this by stripping away all the many factors associated with exercise – such as getting fresh air, being in nature and the satisfaction of reaching fitness goals.

Essentially, ‘movement not only causes increased positive affect [emotional feelings] … but movement partially embodies, or in a sense reflects, positive affect,’ the study authors from The Iowa State University wrote in the paper published in the journal Emotion.

How the research was carried out

Across three studies, the team tested hundreds of undergraduate students who were not aware of the true aims of the research to avoid biased answers.

Two of the studies showed that students who spent 12 minutes on a group walking tour of campus buildings, or on a dull walking tour on their own of the interior of a campus building, reported more positive mood.

This was compared to another group who sat and looking at photographs of the same campus tour, or watched a video of the same building interior tour.

In a second study, positive mood effects were also found even when researchers induced ‘dread’ in the participants before their walk, by instructing them that after the walk they had to write a two-page essay afterwards.

In the final study, students spent 10 minutes watching a Saatchi Gallery video alone, one, in three groups who were either sitting, standing or walking on a treadmill.

Once again, at the end, the students who’d spent time walking reported more positive mood scores than those who had been sitting or standing.

Authors Jeffrey Miller and Zlatan Krizan wrote: ‘People may underestimate the extent to which just getting off their couch and going for a walk will benefit their mood as they focus on momentarily perceived barriers rather than eventual mood benefits.’

The worrying results from a tuberculosis vaccine trial on monkeys before they tested the treatment on hundreds of babies were ignored by scientists at Oxford University, a former principal research fellow at the institution has claimed.

Professor Peter Beverley said that plans to inoculate almost 1,500 children were drawn up without disclosing data that seemed to show that primates given the immunisation in a trial appeared to “die rather rapidly”.

He told the BBC’s File on Four that it “seemed a little bit strange” that most of the primates treated with the vaccine were having to be put down after they became ill.

“Certainly here in this experiment, there is no evidence whatsoever that this is an effective booster vaccine,” he said.

Trials on monkeys saw all of them infected with TB. However, one group was given the widely used Bacillus Calmette-Guérin (BCG) jab, the second as given no immunisation and a third was given BCG plus new vaccine.

The trial had started 10 months before a funding application was made for the clinical trial on over 2,800 babies near Cape Town. Almost half of the infants taking part were given the new vaccine.

By that time, of the six monkeys who received only the BCG injection, just two died, while five out of six of those that received the BCG jab and the new booster vaccine together had to be put down.

Professor Beverley claimed regulators were not given this information when they came to assess the application.

The university insisted that all of the data from the study was shared with the South African regulators. It pointed to the fact that the vaccine had already passed the animal testing phase and had been safely tested on 424 people before the 2009 study began.

Researchers concluded that the amount of TB bacteria used in the study was too high, which lead to the high level of fatalities among monkeys given the vaccine, they said.

Public Health England said that since it was not a pre-clinical trial to support the progression of the vaccine into humans, but instead a separate trial that would inform future animal tests, the results were not relaeant.

An investigation into Professor Beverley’s complaint found no wrongdoing took place.

But it concluded that it “would have been good practice for the potentially adverse reaction observed in the monkey experiment to be reported to the authorities in a more timely fashion.”

Opening a new era in cancer care, US health officials have approved a breakthrough treatment that genetically engineers patients’ own blood cells into an army of assassins to seek and destroy childhood leukaemia.

The Food and Drug Administration called the approval historic, the first gene therapy to hit the US market. Made from scratch for every patient, it’s one of a wave of “living drugs” under development to fight additional blood cancers and other tumours, too.

Novartis Pharmaceuticals set the price for its one-time infusion of so-called “CAR-T cells” at $475,000, but said there would be no charge for patients who didn’t show a response within a month.

“This is a brand new way of treating cancer,” said Dr Stephan Grupp of Children’s Hospital of Philadelphia, who treated the first child with CAR-T cell therapy — a girl who’d been near death but now is cancer-free for five years and counting. “That’s enormously exciting.”

​CAR-T treatment uses gene therapy techniques not to fix disease-causing genes but to turbocharge T cells, immune system soldiers that cancer too often can evade. Researchers filter those cells from a patient’s blood, reprogramme them to harbour a “chimeric antigen receptor” or CAR that zeroes in on cancer, and grow hundreds of millions of copies. Returned to the patient, the revved-up cells can continue multiplying to fight disease for months or years.

It’s a completely different way to harness the immune system than popular immunotherapy drugs called “checkpoint inhibitors” that treat a variety of cancers by helping the body’s natural T cells better spot tumours. CAR-T cell therapy gives patients stronger T cells to do that job.

“We’re entering a new frontier in medical innovation with the ability to reprogramme a patient’s own cells to attack a deadly cancer,” said FDA Commissioner Scott Gottlieb.

The first CAR-T version, developed by Novartis and the University of Pennsylvania, is approved for use by several hundred patients a year who are desperately ill with acute lymphoblastic leukaemia, or ALL. It strikes more than 3,000 children and young adults in the U.S. each year and while most survive, about 15 percent relapse despite today’s best treatments.

In a key study of 63 advanced patients, 83 percent went into remission soon after receiving the CAR-T cells. Importantly, it’s not clear how long that benefit lasts: Some patients did relapse months later. The others still are being tracked to see how they fare long-term.

Still, “a far higher percentage of patients go into remission with this therapy than anything else we’ve seen to date with relapsed leukaemia,” said Dr. Ted Laetsch of the University of Texas Southwestern Medical Center, one of the study sites. “I wouldn’t say we know for sure how many will be cured yet by this therapy. There certainly is a hope” that some will be.

Most patients suffered side effects that can be gruelling, even life-threatening. An immune overreaction called “cytokine release syndrome” can trigger high fevers, plummeting blood pressure and in severe cases organ damage, side effects that require sophisticated care to help patients without blocking the cancer attack. The FDA designated a treatment for those side effects Wednesday.

“This is remarkable technology,” said Dr Mikkael Sekeres of the American Society of Haematology. But, he cautioned that CAR-T “isn’t a panacea.”

Among concerns, sometimes leukaemia can develop resistance, and sometimes patients worsen while waiting for their new cells, said Sekeres, who directs the Cleveland Clinic’s leukaemia programme and wasn’t involved with CAR-T testing.

“Unfortunately leukaemia grows so rapidly that it can evade even the smartest of our technologies,” he added.

To better ensure patient safety, the FDA is requiring Novartis to offer CAR-T therapy only through medical centers specially trained and certified to handle the complicated treatment. Novartis expects to have 32 centres around the country, mostly in large cities, running by year’s end, with the first 20 offering care within the next month.

Patients’ collected immune cells will be frozen and shipped to a Novartis factory in New Jersey that creates each dose, a process the company says should take about three weeks. The $475,000 price tag doesn’t include the cost of needed hospitalizations, travel to a certified hospital and other expenses.

On a conference call Wednesday, Novartis executives said the company is working with the Medicaid program and private insurers and expects broad coverage, and will offer some financial assistance with such things as travel costs. But they didn’t promise all patients would be able to get the therapy.

For some patients, the new CAR-T therapy might replace bone marrow transplants that cost more than half a million dollars, noted Grupp, who led the Novartis study.

“I don’t want to be an apologist for high drug prices in the US,” Grupp stressed. But if it’s the last treatment they need, “that’s a really significant one-time investment in their wellness, especially in kids who have a whole lifetime ahead of them.”

“This is a turning point in the fight” against ALL, said Penn’s Dr Carl June, who pioneered the therapy.

But he and other researchers say thousands more patients eventually may benefit. Kite Pharma’s similar CAR-T brand, developed by the National Cancer Institute, is expected to win approval later this year to treat aggressive lymphoma, and Juno Therapeutics and other companies are studying their own versions against blood cancers including multiple myeloma.

Scientists around the country also are trying to make CAR-T therapies that could fight more common solid tumours such as brain, breast or pancreatic cancers — a harder next step.

“Although narrow in scope, today’s FDA ruling is a milestone,” said Dr. David Maloney of the Fred Hutchinson Cancer Research Center in Seattle, whose team has worked with Juno and is researching CAR-T in a variety of cancers. “Approvals are an important step, but they’re just the beginning.”

Genetic variations linked to illnesses less likely to endure in people who live longer, who in turn are more likely to pass on their genes, new research suggests.

Genes linked to Alzheimer’s disease, asthma and high cholesterol are being “weeded out” by natural selection, a study has found.

Scientists at Cambridge and Colombia universities discovered that genetic variations associated with these illnesses were less common in people who lived longer.

Those who survive to an older age are more likely to successfully pass on their genes than people who die relatively young, the researchers said, and therefore these traits for good health become more common in the human gene pool.

The study, published in the journal PLOS Biology, suggested that natural selection is slowly eliminating negative traits to adapt to our changing lifestyle.

It said even genetic variants with late onset effects, such as those linked to Alzheimer’s, were being “weeded out”.

“It’s a subtle signal, but we find genetic evidence that natural selection is happening in modern human populations,” said Joseph Pickrell, one of the study’s authors.

In theory, illnesses such as Alzheimer’s could be wiped out of the human species within a few thousand years.

The team studied the genetic make-up of 150,000 Britons and 60,000 Americans to analyse human evolution.

It also discovered that people who were genetically pre-disposed to hitting puberty later and those who had their first child later in life were living longer.

A one-year delay in puberty lowered the death rate by 3-4%, while a one-year child-bearing delay lowered the death rate by 6%.

The researchers said traits linked to longer lifespans now may not be useful in the future as conditions change.

To better understand genetic mutations and why they arise, researchers will need to study “millions of samples in the pipeline”, they said.